Department of Ophthalmology, University of Washington , Seattle, Washington.
J Ocul Pharmacol Ther. 2014 Mar-Apr;30(2-3):88-93. doi: 10.1089/jop.2013.0224. Epub 2013 Dec 21.
Intraocular pressure (IOP) is the only treatable risk factor in glaucoma, one of the world's leading causes of blindness. Mechanisms that maintain IOP within a normal range have been poorly understood in contrast to intrinsic mechanisms that regulate systemic blood pressure. Vessel walls experience continuous pulse-induced cyclic pressure and flow. Pressure-dependent wall stress and flow-dependent shear stress provide sensory signals that initiate mechanotransduction responses. The responses optimize vessel wall elasticity, compliance and lumen size, providing a feedback loop to maintain intrinsic pressure homeostasis. Aqueous humor is part of a vascular circulatory loop, being secreted into the anterior chamber of the eye from the vasculature, then returning to the vasculature by passing through the trabecular meshwork (TM), a uniquely modified vessel wall interposed between the anterior chamber and a vascular sinus called Schlemm's canal (SC). Since pressure in circulatory loops elsewhere is modulated by cyclic stresses, one might predict similar pressure modulation in the aqueous outflow system. Recent laboratory evidence in fact demonstrates that cyclic IOP changes alter aqueous outflow while increasing cellularity and contractility of TM cells. Cyclic changes also lead to alterations in gene expression, changes in cytoskeletal networks and modulation of signal transduction. A new technology, phase-based optical coherence tomography, demonstrates in vivo pulse-dependent TM motion like that elsewhere in the vasculature. Recognition of pulse-dependent TM motion provides a linkage to well-characterized mechanisms that provide pressure homeostasis in the systemic vasculature. The linkage may permit unifying concepts of pressure control and provide new insights into IOP homeostatic mechanisms.
眼压（IOP）是青光眼这一全球主要致盲眼病的唯一可治疗的风险因素。与调节全身血压的内在机制相比，维持正常 IOP 的机制尚未得到充分理解。血管壁会持续受到脉搏引起的周期性压力和血流的影响。压力依赖性壁应力和流动依赖性切应力提供了起始机械转导反应的感觉信号。这些反应优化了血管壁的弹性、顺应性和管腔大小，提供了一个反馈回路来维持内在的压力平衡。房水是血管循环回路的一部分，从前房血管中分泌出来，然后通过小梁网（TM）返回血管，TM 是一种独特的血管壁，夹在前房和一个称为施莱姆氏管（SC）的血管窦之间。由于其他循环回路中的压力受到周期性压力的调节，人们可能会预测到类似的房水流出系统中的压力调节。事实上，最近的实验室证据表明，周期性的 IOP 变化会改变房水流出，同时增加 TM 细胞的细胞活力和收缩力。周期性变化还会导致基因表达的改变、细胞骨架网络的改变和信号转导的调节。一种新的技术，基于相位的光学相干断层扫描，在活体中显示出与血管中其他部位相似的依赖于脉冲的 TM 运动。对依赖于脉冲的 TM 运动的识别为提供了与全身血管中压力平衡的特征机制的联系。这种联系可能允许对压力控制的统一概念，并为 IOP 稳态机制提供新的见解。
